Koch K C, vom Dahl J, Kleinhans E, Klues H G, Radke P W, Ninnemann S, Schulz G, Buell U, Hanrath P
Department of Cardiology, University Hospital, University of Technology, Aachen, Germany.
J Am Coll Cardiol. 1999 Mar 15;33(4):998-1004. doi: 10.1016/s0735-1097(98)00659-7.
This study evaluated the effect of the glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist abciximab on myocardial hypoperfusion during percutaneous transluminal rotational atherectomy (PTRA).
PTRA may cause transient ischemia and periprocedural myocardial injury. A platelet-dependent risk of non-Q-wave infarctions after directional atherectomy has been described. The role of platelets for the incidence and severity of myocardial hypoperfusion during PTRA is unknown.
Seventy-five consecutive patients with complex lesions were studied using resting Tc-99m sestamibi single-photon emission computed tomography prior to PTRA, during, and 2 days after the procedure. The last 30 patients received periprocedural abciximab (group A) and their results were compared to the remaining 45 patients (group B). For semiquantitative analysis, myocardial perfusion in 24 left ventricular regions was expressed as percentage of maximal sestamibi uptake.
Baseline characteristics did not differ between the groups. Transient perfusion defects were observed in 39/45 (87%) patients of group B, but only in 10/30 (33%) patients of group A (p < 0.001). Perfusion was significantly reduced during PTRA in 3.3 +/- 2.5 regions in group B compared to 1.4 +/- 2.5 regions in group A (p < 0.01). Perfusion in the region with maximal reduction during PTRA in groups B and A was 76 +/- 15% and 76 +/- 15% at baseline, decreased to 56 +/- 16% (p < 0.001) and 67 +/- 14%, respectively, during PTRA (p < 0.01 A vs. B), and returned to 76 +/- 15% and 80 +/- 13%, respectively, after PTRA. Nine patients in group B (20%) and two patients in group A (7%) had mild creatine kinase and/or troponin t elevations (p = 0.18). Patients with elevated enzymes had larger perfusion defects than did patients without myocardial injury (4.2 +/- 2.7 vs. 2.3 +/- 2.5 regions, p < 0.05).
These data indicate that GPIIb/IIIa blockade reduces incidence, extent and severity of transient hypoperfusion during PTRA. Thus, platelet aggregation may play an important role for PTRA-induced hypoperfusion.
本研究评估糖蛋白IIb/IIIa（GPIIb/IIIa）拮抗剂阿昔单抗对经皮腔内旋切术（PTRA）期间心肌灌注不足的影响。
PTRA可能导致短暂性缺血和围手术期心肌损伤。已描述了定向旋切术后非Q波梗死的血小板依赖性风险。血小板在PTRA期间心肌灌注不足的发生率和严重程度方面的作用尚不清楚。
对75例连续的复杂病变患者在PTRA术前、术中及术后2天使用静息态锝-99m甲氧基异丁基异腈单光子发射计算机断层扫描进行研究。最后30例患者在围手术期接受阿昔单抗治疗（A组），并将其结果与其余45例患者（B组）进行比较。对于半定量分析，24个左心室区域的心肌灌注以最大甲氧基异丁基异腈摄取的百分比表示。
两组患者的基线特征无差异。B组45例患者中有39例（87%）观察到短暂性灌注缺损，而A组30例患者中仅10例（33%）出现（p<0.001）。与A组的1.4±2.5个区域相比，B组在PTRA期间3.3±2.5个区域的灌注显著降低（p<0.01）。B组和A组在PTRA期间灌注降低最大区域的基线灌注分别为76±15%和76±15%，在PTRA期间分别降至56±16%（p<0.001）和67±14%（A组与B组相比，p<0.01），PTRA术后分别恢复至76±15%和80±13%。B组9例患者（20%）和A组2例患者（7%）的肌酸激酶和/或肌钙蛋白t轻度升高（p = 0.18）。酶升高的患者比无心肌损伤的患者有更大的灌注缺损（4.2±2.7个区域对2.3±2.5个区域，p<0.05）。
这些数据表明，GPIIb/IIIa阻断可降低PTRA期间短暂性灌注不足的发生率、范围和严重程度。因此，血小板聚集可能在PTRA诱导的灌注不足中起重要作用。
